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Spinal CordAnatomical and Physiological Features
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The three main ascending spinal tracts are (i) dorsal column medial lemniscus pathway, (ii) spinothalamic tract and (iii) spinocerebellar tract. The dorsal column medial lemniscus conveys information for the perception of pressure, vibration and texture via Aα/β fibres to facilitate discriminative touch. The spinothalamic tract conveys pain and temperature modalities via Aδ/C fibres. Proprioception is conveyed via Aα fibres which terminate at the cerebellum by the spinocerebellar tract. Details of the course of the ascending tracts are described in Chapter 8.
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
All authors of consulted recent texts in neuroanatomy agree that some cerebellar afferents enter in or near the superior cerebellar peduncle (SCP).1 The issue is whether those afferents enter as part of the SCP. In one place or another, many authors define or describe the SCP as containing only efferents, from the cerebellar deep nuclei2 (e.g., C&S, p. 403; Lock, p. 113; Car, p. 126; Hensyl, 1982, p. 1044; CH&L, p. 206–207; M&F, p. 86; A&B, p. 165; Friel, 1981, p. 980). Authors who are internally consistent on this point describe how the ventral spinocerebellar tract enters the cerebellum in various ways: “along the dorsolateral border of” the SCP (C&s, p. 403), “over the dorsal surface of” the SCP (Hensyl, 1982, p. 1471), “alongside” the SCP (Gar, p. 126), “at the side of” the SCP (CH&L, p. 207), or “it loops over” the SCP (Lock, p. 145). Authors of at least one text also describe tectocerebellar fibers as entering the cerebellum “through the anterior medullary velum,” which stretches medially between the two SCP’s, and describe trigeminocerebellar fibers as entering “along the margins of the anterior medullary velum” (CH&L, p. 207–208). Inconsistent authors, on the other hand, describe the ventral spinocerebellar tract, or sometimes other cerebellar afferents, as entering the cerebellum “via” or “by way of” the SCP (e.g., M&F, p. 86; A&B, p. 87; Friel, 1981, p. 1384).
Station 2: History Taking
Published in Saira Ghafur, Parminder K Judge, Richard Kitchen, Samuel Blows, Fiona Moss, The MRCP PACES Handbook, 2017
Saira Ghafur, Parminder K Judge, Richard Kitchen, Samuel Blows, Fiona Moss
What is Friedreich’s ataxia? Autosomal recessive disorder; a trinucleotide repeat on chromosome 9.Degeneration of the spinocerebellar tract resulting in cerebellar signs.Corticospinal tract damage and peripheral nerve degeneration lead to absent ankle jerks with extensor plantars.Pes cavus, scoliosis and diabetes are common features. Other features include cardiomyopathy, cataracts and sensorineural deafness.Think of this in a younger patient.
Center of pressure velocities in patients with body lateropulsion: three case report series of Wallenberg’s syndrome
Published in Physiotherapy Theory and Practice, 2022
Hideaki Matsuo, Masafumi Kubota, Mayumi Matsumura, Mami Takayama, Yuri Mae, Yuki Kitazaki, Soichi Enomoto, Asako Ueno, Masamichi Ikawa, Tadanori Hamano, Ai Takahashi, Misao Tsubokawa, Seiichiro Shimada
Wallenberg’s syndrome, also known as a lateral medullary syndrome, is a neurological condition caused by a lateral medullary infarction. This syndrome’s symptoms are ipsilateral Horner syndrome, ipsilateral limb ataxia, superficial sensory disturbance of the ipsilateral face and contralateral limbs, dysarthria, dysphagia, and vertigo. Body lateropulsion (BL), a postural disorder characterized by the body involuntarily tilting to one side, is one of the Wallenberg syndrome’s predominant symptoms (Dieterich and Brandt, 1992, 2019; Kim et al., 2007; Maeda et al., 2005; Pérennou et al., 2008; Thömke et al., 2005; Yamaoka, Kishishita, Takayama, and Okubo, 2018). Lesions of the descending lateral vestibulospinal tract or the ascending dorsal spinocerebellar tract may induce BL (Kim et al., 2007; Maeda et al., 2005; Thömke et al., 2005). Pérennou et al. (2008) reported that patients having brainstem strokes showed severe visual vertical tilts and BL and minor or no tilts of vertical posture. This suggests that vestibular nuclear lesions interfere with postural control via direct vestibulo-spinal mechanisms rather than via a higher-order representation mechanism (Kim et al., 2007; Pérennou et al., 2008, 2014). Although pathological mechanisms that cause BL are better understood, features of postural control are not fully understood. Therefore, demonstrating these features during the recovery process of patients with BL may assist in developing effective physical therapy programs and plans of care.